Research advances on the role of Na+-K+-ATPase regulation in pulmonary edema clearance of acute respiratory distress syndrome

Abstract

Acute respiratory distress syndrome (ARDS) is a critical disease with high mortality, and currently there is no specific treatment. ARDS is characterized by refractory hypoxemia secondary to pulmonary edema, but the underlying mechanism is not yet fully understood. Alveolar edema fluid is mainly actively transported and reabsorbed by sodium-water transport system. The sodium pump (Na+-K+-ATPase-mediated Na+ transport) on the basal side of type II alveolar epithelial cells (AT II) is the main driving force for pulmonary edema clearance. Na+-K+-ATPase regulation is affected by many regulatory factors through a variety of ways, among which "long-term regulation" mechanism plays an important role, including positively regulating the gene transcription and protein expression of Na+-K+-ATPase. Na+-K+-ATPase can also be degraded by ubiquitin-proteasome pathway (UPP) and autophagy lysosome pathway to affect its abundance and enzyme activity, meanwhile, Na+-K+-ATPase α1 plays a key role in sodium water transport. We review the "long-term regulation" mechanism of Na+-K+-ATPase related pathways in pulmonary edema clearance and explore the possibility of new therapies for ARDS based on this mechanism, so as to provide new targets for the treatment of ARDS.